获能是正常生理条件下人精子顶体反应及受精的必要前提，离子通道参与调控精子获能。钾离子通道KCNQ1常与KCNE家族辅助亚基相互作用，形成KCNQ1/KCNE通道，具有调控细胞膜电位、调节其他离子转运驱动力等重要功能。我们前期研究发现，KCNQ1在人精子中表达，其特异性抑制剂Chromanol 293B可影响精子获能后的超激活运动，提示该离子通道参与调控精子获能，但分子机制不明。本项目拟围绕KCNQ1及KCNE家族蛋白开展四个层面研究：确定KCNE家族成员在人精子中的表达和定位；明确人精子中哪些KCNE家族成员与KCNQ1相互作用；明确KCNQ1/KCNE通道是否参与调控精子获能、影响受精；阐明其是否通过调节精子细胞膜电位、调控其他离子的转运驱动力进而影响获能。本项目旨在揭示KCNQ1及其KCNE家族辅助亚基调控人精子获能进而影响受精的机制，为填补精子获能调控理论及诊治男性不育提供科学依据。

Human sperm capacitation is a prerequisite for acrosome reaction, sperm-egg fusion and fertilization under normal physiological conditions. This physiological process is regulated by ion channels. Potassium channel KCNQ1 always interacts with KCNE family auxiliary subunits, they play important roles in regulation of cell membrane potential, osmotic pressure and transfer driving force of other ions. In the previous studies, we found that KCNQ1 was expressed in human sperm. Further studies indicated that chromanol 293B, the specific inhibitor of KCNQ1, effected hyperactivated motility of human sperm. These results suggest that potassium channel KCNQ1 participates in regulation of human sperm capacitation, however the molecular mechanism is still unknown. Therefore, in this study we focus on potassium channel KCNQ1 and its KCNE family auxiliary subunits to detect the expression and location of KCNE family members in human sperm; which members of KCNE family auxiliary subunits interact with KCNQ1 during huamn sperm capacitation; whether KCNQ1/KCNE potassium channel participates in regulation of human sperm capacitation; what the molecular mechanism of KCNQ1/KCNE during capacitation is. The results of the study will reveal the mechanism of KCNQ1 and KCNE family auxiliary subunits in regulating human sperm capacitation. This will improve the regulation network of sperm capacitation and provide new theory for diagnosis and treatment of unexplained male infertility.